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. 2015 Sep 3;9:235. doi: 10.3389/fnbeh.2015.00235

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Copyright © 2015 Häring, Enk, Rey, Loch, de Azua, Weber, Bartsch, Monory and Lutz.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution and reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Tamoxifen-inducible genetic inactivation of cannabinoid type 1 (CB₁) receptor in TPH2-positive neurons. (A) Schematic illustrations of CB₁^fl/fl allele before (above) and after Cre recombinase-mediated recombination (below). Arrows indicate primer positions. (B) Applying primers G50/G53, polymerase chain reaction (PCR) reactions were run using genomic DNA from the raphe nuclei region as a template. The 600 bp band indicating successful recombination was only detected in mice containing the CreER^T2 transgene. (Cre+) after treatment with tamoxifen (+Tam). LA, left homology arm; RA, right homology arm; Cre+, animals heterozygous for the CreER^T2 transgene and homozygous for the CB₁^fl/fl allele. Cre- = CB₁^fl/fl mice without the CreER^T2 transgene; +Tam, tamoxifen-treated; −Tam, vehicle-treated; M, DNA size marker.

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